Kozàkovà M, Palombo C, Pratali L, Pittella G, Galetta F, L'Abbate A
Institute of Clinical Physiology, National Research Council (CNR), Pisa, Italy.
Hypertension. 1997 Feb;29(2):551-9. doi: 10.1161/01.hyp.29.2.551.
The purpose of this study was to investigate the different mechanisms responsible for an impairment of coronary vasodilator capacity in hypertensive subjects by an integrated echocardiographic approach, including transesophageal Doppler echocardiography, which allows noninvasive monitoring of coronary flow velocity in the left anterior descending artery during pharmacological vasodilation. The study population consisted of 17 healthy control subjects and 33 hypertensive subjects: 10 without hypertrophy, 16 with mild to moderate hypertrophy, and 7 with severe left ventricular hypertrophy. Mean systolic and diastolic flow velocities were monitored basally (together with indexes of myocardial oxygen demand, such as heart rate, myocardial inotropism, and left ventricular wall stress) and during infusion of low-dose (0.56 mg/kg per 4 minutes) and high-dose (0.84 mg/kg per 9 minutes) dipyridamole. Coronary reserve was assessed as the ratio of mean diastolic velocity after high-dose dipyridamole and basal diastolic velocity, and minimum coronary resistance as the ratio of diastolic blood pressure and diastolic velocity after high-dose dipyridamole. Compared with the control group, in all hypertensive groups, coronary reserve was similarly decreased (3.54 +/- 0.84 versus 2.59 +/- 0.42, 2.29 +/- 0.46, and 2.43 +/- 0.71; P < .01) and minimum resistance increased (0.56 +/- 0.15 versus 0.75 +/- 0.31, 0.75 +/- 0.19, and 0.78 +/- 0.21 mm Hg.s-1.cm-1; P = NS). These results confirm that coronary reserve in hypertensive individuals is reduced even before the occurrence of left ventricular hypertrophy. The reduction in coronary reserve depends on both an increase in resting coronary flow and an impairment in maximal vasodilator capacity. An increase in resting flow is dependent on higher heart rate and wall stress in hypertensive subjects without ventricular hypertrophy and on increased myocardial mass in hypertensive subjects with hypertrophy. Hypertensive subjects with ventricular hypertrophy also demonstrated a significantly blunted response to low-dose dipyridamole.
本研究的目的是通过一种综合超声心动图方法，包括经食管多普勒超声心动图，来探究导致高血压患者冠状动脉舒张能力受损的不同机制。经食管多普勒超声心动图能够在药物血管舒张期间对左前降支冠状动脉血流速度进行无创监测。研究人群包括17名健康对照者和33名高血压患者：10名无心肌肥厚，16名有轻度至中度心肌肥厚，7名有严重左心室肥厚。在基础状态下（同时监测心肌需氧量指标，如心率、心肌收缩力和左心室壁应力）以及输注低剂量（每4分钟0.56 mg/kg）和高剂量（每9分钟0.84 mg/kg）双嘧达莫期间，监测平均收缩期和舒张期血流速度。冠状动脉储备通过高剂量双嘧达莫后平均舒张期速度与基础舒张期速度之比来评估，最小冠状动脉阻力通过舒张压与高剂量双嘧达莫后舒张期速度之比来评估。与对照组相比，在所有高血压组中，冠状动脉储备均同样降低（3.54±0.84对2.59±0.42、2.29±0.46和2.43±0.71；P<0.01），最小阻力增加（0.56±0.15对0.75±0.31、0.75±0.19和0.78±0.21 mmHg·s⁻¹·cm⁻¹；P=无显著性差异）。这些结果证实，即使在左心室肥厚发生之前，高血压个体的冠状动脉储备就已降低。冠状动脉储备的降低既取决于静息冠状动脉血流的增加，也取决于最大血管舒张能力的受损。静息血流的增加在无心室肥厚的高血压患者中取决于较高的心率和壁应力，在有心肌肥厚的高血压患者中取决于心肌质量的增加。有心室肥厚的高血压患者对低剂量双嘧达莫的反应也明显减弱。
